1/ Why does LDLc go up more if you're leaner and have higher energy demands, one explaination by @DaveKeto (and hopefully I recount it corrently):
In a low-carb state, dependence on fat metabolism is increased. Thus, ur fat cells r shrinking& growing in a more dynamic fashion...
2/ In order to expand, the fat cell (and other cells) needs material that can be provided by circulating lipoproteins.
Now let's pause and remeber that leanness & metabolic health are characterized by small fat cells (even if there are more). This is healthy but...
3/ If you fat cell is small its going to have a higher surface area to volume ratio than large fat cells. Thus, to grow and the same amount in terms of volume (as the TG pool is turned over more quickly) small fat cells will require more membrane components provided by LDL...
4/ Thus both lower fat cell size and higher demand to shrink and grow more dyanmically (higher energy needs) would increase LDL as needed. It's speculative at this point but makes sense to me!
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1/ What does Lipid Trafficking and VLDL have to do with type II #diabetes?
Check out my new video on the "Twin Cycle Hypothesis"
In 9 min, you'll be smarter than you were before!
🤓🤓🤓👇👇👇 #LEM#Lipids#Insulin
2/ After you watch the video, can you answer the following "quiz" questions?
(i) How does the contribution of de novo lipogenesis to Triglyceries in VLDL change as liver fat accumulates?
...
3/ T/F and why?
(ii) Palmitic acid is transported by VLDL1 to the pancreas, harming beta cells in the pancreas. Palmitic acid is a major saturated fat (16:0) found in animal foods. So, you should eat less red meat and dairy and substitue in healthy whole grains & fruit, like 🍌?
2/ The twin cycle hypothesis postulates that accumulation of liver fat can drive diabetes in the following way: more liver fat promotes hepatic insulin resistance which increases gluconeogenesis and thus increases insulin to promote more de novo lipogenesis. Basically…
3/ Basically, more liver fat more insulin resistance more liver fat and so on. New human data provide support for the model. One of the key findings of the paper is that more liver fat = more de novo lipogenesis, creating specifically the saturated fat palmitic acid (PA)…
2/ Also, it's all very mechanistic, with ANGPTL4 vs. 3/8 being oppositely regualted by feeding and fasting in a tissue specific manner such that fasting decreases fat storage in adopicytes and feeding promotes it.
And, perhaps, unsuprislingly, the lipid metabolism is...
3/ w.r.t ANGPTLs (and specifically 4, which controls local LPL activity) is linked with glucose homeostasis...
AcAc binds to the GPR43/FFAR2 receptor to promote Lipoprotein Lipase activity and help burn fat.
Some more details...
2/ Short-chain fatty acids (SCFAs) in the gut r known to modulate energy homeostatis. Butyrate, acetate, proprionate all have recptors. The acetate receptor is GPR43.
The ketone BhB is all well studied as a signaling molecule, and binds HCAR2 etc., but AcAc is less well studied.
3/ This paper provides good evidence that, during fasting and ketogenic conditions, its AcAc that helps promote fat burning (lypolysis) throughout the body (except in the gut, more on that in a bit). Again, AcAc binds GPR43 and promotes Lipoprotein lipase (LPL activity)...
New paper tries to claim high inter-individual variability as an excuse for backing the notion that #saturated fat is unhealthy. Things that I thought as I read…
1/ Abstract depicts sat fat as a burger with fries. Sigh...
2/ calls out isocaloric replacement studies 4replacing SAT w carbs rather than PUFA. Fair point, but what practical options r available to people in this world. How r ppl going to read this article? Trade butter for raw tahini, or soybean oil margarine, or go for low-fat cookie?
3/ Cite whole foods complex matrix as a confounding variable. Maybe just say eat whole food and not processed junk? most of American’s sat fat comes from sweets and pasteries, not whole foods. let's just agree the ice cream isn't saving your heart health, don't lump in the steak
1/ What would you predict would happen to fasting triglycerides and LDL if you just ate a TON of fat and Saturated Fat. Like, if you drank 6000 kCal and 1.6 Liters of heavy cream?!
Trigs (fat in blood) and LDL-C would obviously go up right?
2/ Well, if your #keto#lchf not necessarily. In fact, overeating tons of fat can DROP your fasting triglycerides and LDL like a stone! WTF?! So what’s going on…
3/ Well, chylomicrons from the intestines (and VLDL secreted by the liver) carry triglycerides. But their residence time in the blood is very short, such that when you have a fasted lipid test, the fat you ate should have been deposited in storage around your body. BUT…